Figure 10.

Schematic representation of pathomechanistic events in LC3B^−/− mice. Aged LC3B^−/− mice (42 w) lungs show increased cellularity and AECII apoptosis with smaller lamellar body profiles. AECII show increase in syntaxin 17, lysosomal, and ER stress with a concomitant increase in the novel LC3B interacting partner, cathepsin A that contributes to AECII apoptosis. Furthermore, LC3B^−/− mice display increased susceptibility to bleomycin-induced lung injury and fibrosis. Similar observations from the lungs of patients with IPF emphasized the pathomechanistic role of autophagy in lung fibrosis.